Antibodies to gap-junctional protein selectively disrupt junctional communication in the early amphibian embryo

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Abstract
Antibodies to the major protein of rat liver gap junctions, MW 27,000 (27K), were microinjected into 1 identified cell of 8-cell stage Xenopus embryos. This treatment selectively disrupts both dye transfer and electrical coupling between the progeny cells. The 27K protein apparently is an integral component of the cell-to-cell junctional channel. The disruption of junctional communication at early stages results in specific developmental defects, suggesting that blocking intercellular communication can have a pronounced influence on embryonic development.